Figure 2From: Effects of helminth co-infections on atopy, asthma and cytokine production in children living in a poor urban area in Latin AmericaA hypothesis to explain the pattern of cytokine production observed in cultures of peripheral blood leukocytes from individuals who had been infected with multiple helminths, specifically spontaneous production of IL-10 in the absence of exogenous antigen (i.e. in unstimulated cultures); and the presence of a Th2 recall response, but not an IL-10 recall response, to A. lumbricoides antigens. (1) Multiple helminth infections could lead to stimulation of the immune system by hundreds of different antigens, including antigens that are cross-reactive with self antigens. (2) Strong helminth-specific and nonspecific polyclonal Th2 immune responses, with the differentiation and expansion of memory cells, would result from such infections. The Th2 immune response could lead to helminth-specific and non-specific polyclonal IgE production, to eosinophil expansion and activation, and to inflammation. The high levels of polyclonal IgE could theoretically inhibit mast cell activation, by competition with allergen-specific IgE for FcϵRI receptors on mast cells, causing inhibition of immediate hypersensitivity skin test to allergens). (3) A consequent differentiation and expansion of helminth-specific Tregs, some of them cross-reactive with self antigens (and some perhaps only autoantigen-reactive, as a consequence of tissue damage by inflammation) could occur (for the sake of clarity, only cross-reactive and helminth-specific Tregs are shown). (4) The cross-reactive/self antigen-specific Tregs would be maintained in a steady state of activation by self antigens, and would release low levels of regulatory cytokines, including IL-10. The spontaneous production of elevated levels of IL-10 could suppress mast-cell degranulation. Because these Tregs could be maintained through continuous stimulation to self antigens in vivo, they would not be further stimulated by helminth antigens in vitro. TLR- toll-like receptor.Back to article page